Idiopathic thrombocytopenic purpura (ITP), neonatal purpura (INT) post-transfusion purpura (PTP), drug-purpura and thrombocytopenia associated with infection or altered immune states are the major immunologic thrombocytopenias. Antibody reactions in these disorders are relevant to autoimmunity, histocompatibility, malignant surveillance, alloimmunity, pathogenicity of antigen-antibody complexes and cellular immune injury generally. We have developed more precise and sensitive assays than heretofore available for platelet-associated (PA) IgG, IgM, IgA and albumin and Western blot analysis (WB) of specific platelet receptors. We found that normal IgG, M and A reacted in WB with receptors of 90kD and 120kD. These receptors were distinct from glycoproteins IIIa and V and were bound to internal membranes. The pathophysiology of post-transfusion purpura (PTP) was found to be compatible with adsorption of antigen- antibody complexes by quantitative adsorption of P1A1 -anti- P1A1 on platelets and by PTP response to plasmapheresis. Neonatal thrombocytopenia cases, as well as PTP cases were a source of antibodies that led to clear identification of the P1A2 antigen, the allele of P1A1. Studies of Ag-Ab complexes, and PAIgG in AIDS, lupus erythematosus, and primary biliary cirrhosis, has helped clarify the mechanism of thrombocytopenia in these diseases. The platelet receptor for drug antibodies was found not to be solely dependent on GPIb, V, and IX as previously supposed.